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Guillain–Barré syndrome

The Guillain–Barré syndrome (GBS) is defined as heterogeneous group of autoimmune polyradiculopathy, involving sensory, motor and autonomic nerves.

Clinical presentation

Classical presentation of GBS includes symmetrical ascending muscle paresis or palsy, areflexia or hyporeflexia along with variable degree of sensory or autonomic involvement.

Most cases are preceded by upper respiratory tract infections or diarrhoea 1-3 weeks before its onset, most commonly caused by Campylobacter jejuni ( ~ 40 % seropositive). Molecular mimicry with the bacterial agents is thought to cause the autoimmunity.

Several sub-types have been described including :

GBS is diagnosed by combination of clinical presentation,CSF study and electrophysiological criteria. CSF abnormalities are characterized by increase protein with pleocytosis. Nerve conduction abnormalities include slow or blocked nerve conduction, prolongation of distal latency and f-waves.GBS is primarily managed with IV immunoglobulins or plasmapharesis along with supportive measures. 

Radiographic features

Radiologic studies are ordered to exclude other causes and in cases where nerve conduction studies and CSF examination are equivocal.

MRI

MRI of the spine is most useful helps excluding other aetiologies like transverse myelitis and compressive causes of polyradiculopathy. Typical findings in a case GBS include nerve root thickening and enhancement surrounding the medullary cone extending along the cauda equina. In the brain the facial nerve is the most commonly affected 1.

These findings are as a result of break down in the blood brain barrier. The most common site of enhancement in GBS is considered to be anterior nerve roots. MRI is a sensitive but non-specific examination diagnoses is reached by correlating clinical findings with patterns of nerve root enhancement and nerve conduction findings.

Differential diagnosis

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